Database : MEDLINE
Search on : Parathyroid and Hormone [Words]
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[PMID]: 29520133
[Au] Autor:Xing W; Lv X; Gao W; Wang J; Yang Z; Wang S; Zhang J; Yan J
[Ad] Address:Zhejiang Provincial Key Laboratory of Geriatrics, Department of Geriatrics, Zhejiang Hospital.
[Ti] Title:Bone mineral density in patients with chronic heart failure: a meta-analysis.
[So] Source:Clin Interv Aging;13:343-353, 2018.
[Is] ISSN:1178-1998
[Cp] Country of publication:New Zealand
[La] Language:eng
[Ab] Abstract:Objective: This study aimed to verify the existing relationship between bone mineral density (BMD) and chronic heart failure (CHF) by meta-analysis. Methods: Databases, including PubMed, Web of Science, and Chinese National Knowledge Infrastructure, published in English or Chinese up to February 28, 2017, were searched for studies on the association between CHF and BMD. Two independent reviewers collected the relevant articles. The standard mean deviation (SMD) and 95% confidence interval were calculated for BMD with fixed- and random-effect models. Subgroup and sensitivity analyses were also conducted. Results: A total of six studies (552 CHF and 243 non-CHF patients) were included. The results indicated that the patients with CHF had a lower total BMD compared with the non-CHF patients. Similar effects were also observed for femoral neck, arm, leg, and trunk BMD. However, no difference was observed in the lumbar spine BMD. The SMD of total BMD in New York Heart Association classes I or II (NYHA I or II) patients was -0.62, while that in NYHA III or IV patients was -0.87, and the SMD of femoral bone mineral density in NYHA I or II patients was -0.47, while that in NYHA III or IV patients was -1.07. Moreover, vitamin D and parathyroid hormone (PTH) were also found to be associated with CHF. Conclusion: Patients with CHF had a lower total BMD and femoral neck, arm, leg, or trochanter BMD than patients with non-CHF. Vitamin D reduced, whereas PTH increased, with the severity of CHF. The clinical significance of the present findings remains uncertain and should be confirmed by future studies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.2147/CIA.S154356

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[PMID]: 29501726
[Au] Autor:Kim BH; Pereverzev A; Zhu S; Tong AOM; Dixon SJ; Chidiac P
[Ad] Address:Department of Physiology and Pharmacology, Schulich School of Medicine & Dentistry, The University of Western Ontario, London, Canada; Bone and Joint Institute, The University of Western Ontario, London, Canada.
[Ti] Title:Extracellular nucleotides enhance agonist potency at the parathyroid hormone 1 receptor.
[So] Source:Cell Signal;46:103-112, 2018 Mar 01.
[Is] ISSN:1873-3913
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Parathyroid hormone (PTH) activates the PTH/PTH-related peptide receptor (PTH1R) on osteoblasts and other target cells. Mechanical stimulation of cells, including osteoblasts, causes release of nucleotides such as ATP into the extracellular fluid. In addition to its role as an energy source, ATP serves as an agonist at P2 receptors and an allosteric regulator of many proteins. We investigated the effects of concentrations of extracellular ATP, comparable to those that activate low affinity P2X7 receptors, on PTH1R signaling. Cyclic AMP levels were monitored in real-time using a bioluminescence reporter and ß-arrestin recruitment to PTH1R was followed using a complementation-based luminescence assay. ATP markedly enhanced cyclic AMP and ß-arrestin signaling as well as downstream activation of CREB. CMP - a nucleotide that lacks a high energy bond and does not activate P2 receptors - mimicked this effect of ATP. Moreover, potentiation was not inhibited by P2 receptor antagonists, including a specific blocker of P2X7. Thus, nucleotide-induced potentiation of signaling pathways was independent of P2 receptor signaling. ATP and CMP reduced the concentration of PTH (1-34) required to produce a half-maximal cyclic AMP or ß-arrestin response, with no evident change in maximal receptor activity. Increased potency was similarly apparent with PTH1R agonists PTH (1-14) and PTH-related peptide (1-34). These observations suggest that extracellular nucleotides increase agonist affinity, efficacy or both, and are consistent with modulation of signaling at the level of the receptor or a closely associated protein. Taken together, our findings establish that ATP enhances PTH1R signaling through a heretofore unrecognized allosteric mechanism.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 41301 MEDLINE  
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[PMID]: 29482068
[Au] Autor:Tajima T; Menuki K; Okuma KF; Tsukamoto M; Fukuda H; Okada Y; Kosugi K; Yamanaka Y; Uchida S; Sakai A
[Ad] Address:Department of Orthpaedic Surgery, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
[Ti] Title:Cortical bone loss due to skeletal unloading in aldehyde dehydrogenase 2 gene knockout mice is associated with decreased PTH receptor expression in osteocytes.
[So] Source:Bone;110:254-266, 2018 Feb 23.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Aldehyde dehydrogenase 2 (ALDH2) is the enzyme that degrades and detoxifies the acetaldehyde produced by alcohol metabolism. In our previous study, we found that compared with wild-type mice (WT), climbing exercises did not increase trabecular bone mass in Aldh2 knockout mice (KO). The purpose of this study was to clarify the effect of the Aldh2 gene on cortical bone structure and on the dynamics of skeletal unloading. Eight-week-old male KO and WT were divided into ground control (GC) or tail suspension (TS) groups for one week (i.e., the KOGC, KOTS, WTGC and WTTS groups). We measured the bone mineral density (BMD) of the femur using dual-energy X-ray absorptiometry. We assessed the femoral morphometry using peripheral quantitative computed tomography (pQCT) and evaluated the femoral cortex histomorphometry, and cortical mRNA using quantitative RT-PCR and cortical bone immunohistostaining. No significant differences were found between the femoral BMD of WTGC and that of WTTS, but the BMD in KOTS was significantly lower than that of KOGC. The pQCT results revealed that the cortical BMD of the femoral diaphysis in KOTS was significantly lower than that of KOGC. Furthermore, the cortical bone area and cortical thickness were significantly lower in KOTS than in the other three groups. Cortical histomorphometric analysis revealed that the endosteal and periosteal bone formation parameters were significantly lower in KOTS than in KOGC. Bone formation signals such as parathyroid hormone receptor (PTHR) were significantly decreased in KOTS compared with the levels in KOGC. Cortical bone immunohistostaining revealed a significantly decreased expression of PTHR in the osteocytes of KOTS compared with the expression level in KOGC. Thus, we concluded that when the Aldh2 gene is disrupted, skeletal unloading suppresses bone formation to decrease cortical bone mass, which may be mediated by a decreased expression of PTH receptors in osteocytes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 41301 MEDLINE  
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[PMID]: 29475111
[Au] Autor:Brent MB; Brüel A; Thomsen JS
[Ad] Address:Department of Biomedicine, Aarhus University, Denmark. Electronic address: mbb@biomed.au.dk.
[Ti] Title:PTH (1-34) and growth hormone in prevention of disuse osteopenia and sarcopenia in rats.
[So] Source:Bone;110:244-253, 2018 Feb 20.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Osteopenia and sarcopenia develops rapidly during disuse. The study investigated whether intermittent parathyroid hormone (1-34) (PTH) and growth hormone (GH) administered alone or in combination could prevent or mitigate disuse osteopenia and sarcopenia in rats. Disuse was achieved by injecting 4IU botulinum toxin A (BTX) into the right hindlimb musculature of 12-14-week-old female Wistar rats. Seventy-two rats were divided into six groups: 1. Baseline; 2. Ctrl; 3. BTX; 4. BTX+GH; 5. BTX+PTH; 6. BTX+PTH+GH. PTH (1-34) (60µg/kg/day) and GH (5mg/kg/day). The animals were sacrificed after 6weeks of treatment. Sarcopenia was established by histomorphometry, while the skeletal properties were determined using DXA, µCT, mechanical testing, and dynamic bone histomorphometry. Disuse resulted in lower muscle mass (-63%, p<0.05), trabecular BV/TV (-28%, p<0.05), Tb.Th (-11%, p<0.05), lower diaphyseal cortical thickness (-10%, p<0.001), and lower bone strength at the distal femoral metaphysis (-27%, p<0.001) compared to Ctrl animals. PTH fully counteracted the immobilization-induced lower BV/TV, Tb.Th, and distal femoral metaphyseal strength. GH increased muscle mass (+17%, p<0.05) compared to BTX, but did not prevent the immobilization-induced loss of bone strength, BV/TV, and cortical trabecular thickness. Combination of PTH and GH increased distal femoral metaphyseal bone strength (+45%, p<0.001), BV/TV (+50%, p<0.05), Tb.Th (+40%, p<0.05), and whole femoral aBMD (+15%, p<0.001) compared to BTX and muscle mass (+21%, p<0.05) compared to BTX+PTH. In conclusion, PTH and GH in combination is more efficient at preventing the disuse-related deterioration of bone strength, density, and micro-architecture than either PTH or GH given as monotherapy. Furthermore, GH, either alone or in combination with PTH, attenuated disuse-induced loss of muscle mass. The combination of PTH and GH resulted in a more effective treatment than PTH and GH as monotherapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 41301 MEDLINE  
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[PMID]: 29471062
[Au] Autor:Karaca A; Malladi VR; Zhu Y; Tafaj O; Paltrinieri E; Wu JY; He Q; Bastepe M
[Ad] Address:Endocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
[Ti] Title:Constitutive stimulatory G protein activity in limb mesenchyme impairs bone growth.
[So] Source:Bone;110:230-237, 2018 Feb 20.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:GNAS mutations leading to constitutively active stimulatory G protein alpha-subunit (Gsα) cause different tumors, fibrous dysplasia of bone, and McCune-Albright syndrome, which are typically not associated with short stature. Enhanced signaling of the parathyroid hormone/parathyroid hormone-related peptide receptor, which couples to multiple G proteins including Gsα, leads to short bones with delayed endochondral ossification. It has remained unknown whether constitutive Gsα activity also impairs bone growth. Here we generated mice expressing a constitutively active Gsα mutant (Gsα-R201H) conditionally upon Cre recombinase (cGsα mice). Gsα-R201H was expressed in cultured bone marrow stromal cells from cGsα mice upon adenoviral-Cre transduction. When crossed with mice in which Cre is expressed in a tamoxifen-regulatable fashion (CAGGCre-ER™), tamoxifen injection resulted in mosaic expression of the transgene in double mutant offspring. We then crossed the cGsα mice with Prx1-Cre mice, in which Cre is expressed in early limb-bud mesenchyme. The double mutant offspring displayed short limbs at birth, with narrow hypertrophic chondrocyte zones in growth plates and delayed formation of secondary ossification center. Consistent with enhanced Gsα signaling, bone marrow stromal cells from these mice demonstrated increased levels of c-fos mRNA. Our findings indicate that constitutive Gsα activity during limb development disrupts endochondral ossification and bone growth. Given that Gsα haploinsufficiency also leads to short bones, as in patients with Albright's hereditary osteodystrophy, these results suggest that a tight control of Gsα activity is essential for normal growth plate physiology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  6 / 41301 MEDLINE  
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[PMID]: 29467330
[Au] Autor:Christov M; Clark AR; Corbin B; Hakroush S; Rhee EP; Saito H; Brooks D; Hesse E; Bouxsein M; Galjart N; Jung JY; Mundel P; Jüppner H; Weins A; Greka A
[Ad] Address:Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
[Ti] Title:Inducible podocyte-specific deletion of CTCF drives progressive kidney disease and bone abnormalities.
[So] Source:JCI Insight;3(4), 2018 Feb 22.
[Is] ISSN:2379-3708
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Progressive chronic kidney diseases (CKDs) are on the rise worldwide. However, the sequence of events resulting in CKD progression remain poorly understood. Animal models of CKD exploring these issues are confounded by systemic toxicities or surgical interventions to acutely induce kidney injury. Here we report the generation of a CKD mouse model through the inducible podocyte-specific ablation of an essential endogenous molecule, the chromatin structure regulator CCCTC-binding factor (CTCF), which leads to rapid podocyte loss (iCTCFpod-/-). As a consequence, iCTCFpod-/- mice develop severe progressive albuminuria, hyperlipidemia, hypoalbuminemia, and impairment of renal function, and die within 8-10 weeks. CKD progression in iCTCFpod-/- mice leads to high serum phosphate and elevations in fibroblast growth factor 23 (FGF23) and parathyroid hormone that rapidly cause bone mineralization defects, increased bone resorption, and bone loss. Dissection of the timeline leading to glomerular pathology in this CKD model led to the surprising observation that podocyte ablation and the resulting glomerular filter destruction is sufficient to drive progressive CKD and osteodystrophy in the absence of interstitial fibrosis. This work introduces an animal model with significant advantages for the study of CKD progression, and it highlights the need for podocyte-protective strategies for future kidney therapeutics.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  7 / 41301 MEDLINE  
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[PMID]: 29428552
[Au] Autor:De Luna G; Ranque B; Courbebaisse M; Ribeil JA; Khimoud D; Dupeux S; Silvera J; Offredo L; Pouchot J; Arlet JB
[Ad] Address:Internal Medicine Department, Sickle Cell Referral Center, Georges Pompidou European Hospital, AP-HP, Paris, France; Faculté de Médecine Paris Descartes, Sorbonne Paris-Cité, Paris, France. Electronic address: gonzalo.deluna@aphp.fr.
[Ti] Title:High bone mineral density in sickle cell disease: Prevalence and characteristics.
[So] Source:Bone;110:199-203, 2018 Feb 08.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Osteosclerosis (OSC) is a rarely studied complication of sickle cell disease (SCD). The objective of our study was to determine the prevalence and characteristics of high bone mineral density (BMD) and its radiological features in adult SCD patients. METHODS: This prospective observational study was conducted from May 2007 to May 2016 in consecutive patients with steady-state SCD at two university hospitals. The BMD of the lumbar spine (L1-L4) and right femoral neck was determined by dual energy X-ray absorptiometry. Clinical, laboratory and radiographic data were recorded. High BMD was defined as a BMD Z-score of at least +2.5 standard deviations at the lumbar spine or hip. The characteristics of the patients with high BMD were compared to those of individuals with low or middle BMD, using multivariate ordinal logistic regression. RESULTS: 135 patients (86 women and 49 men) with a median age of 27 (IQR 23-33) years were included. High BMD was diagnosed in 20 (15%) patients with a median age of 33.5 (IQR 28-45) years. The SCD genotypes of these patients were SS in 11, SC in 5, S/beta+ in 3, and S/beta0 in 1. High BMD patients more frequently harbored the S/beta SCD genotype (21% vs 5% in non-high BMD patients; p=0.047) and were older (p=0.0007). Compared to patients with low or middle BMD, after adjustment for age and SCD genotype, high BMD patients had a higher prevalence of avascular necrosis history (p=0.009), higher BMI (p=0.007), and lower serum resorption marker CTX (p=0.04), bilirubin (p=0.02) and parathyroid hormone levels (p=0.02). There were no differences between groups regarding fracture history, H-shaped vertebrae or other biological variables. CONCLUSION: High-BMD values is a common manifestation in SCD patients, especially in those with the S/beta-thalassemia genotypes. The prevalence of high-BMD in SCD is associated with older age, suggesting that it will be more common in the future because the life span of patients with SCD is increasing thanks to significant progress in SCD treatment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 41301 MEDLINE  
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[PMID]: 29408411
[Au] Autor:Yukata K; Xie C; Li TF; Brown ML; Kanchiku T; Zhang X; Awad HA; Schwarz EM; Beck CA; Jonason JH; O'Keefe RJ
[Ad] Address:Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY, USA; Department of Orthopedic Surgery, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
[Ti] Title:Teriparatide (human PTH ) compensates for impaired fracture healing in COX-2 deficient mice.
[So] Source:Bone;110:150-159, 2018 Feb 03.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Genetic ablation of cyclooxygenase-2 (COX-2) in mice is known to impair fracture healing. To determine if teriparatide (human PTH ) can promote healing of Cox-2-deficient fractures, we performed detailed in vivo analyses using a murine stabilized tibia fracture model. Periosteal progenitor cell proliferation as well as bony callus formation was markedly reduced in Cox-2 mice at day 10 post-fracture. Remarkably, intermittent PTH administration increased proliferation of periosteal progenitor cells, restored callus formation on day 7, and enhanced bone formation on days 10, 14 and 21 in Cox-2-deficient mice. PTH also increased biomechanical torsional properties at days 10 or 14 in all genotypes, consistent with enhanced bony callus formation by radiologic examinations. To determine the effects of intermittent PTH for callus remodeling, TRAP staining was performed. Intermittent PTH treatment increased the number of TRAP positive cells per total callus area on day 21 in Cox-2 fractures. Taken together, the present findings indicate that intermittent PTH treatment could compensate for COX-2 deficiency and improve impaired fracture healing in Cox-2-deficient mice.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 41301 MEDLINE  
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[PMID]: 29340678
[Au] Autor:Ikramuddin S; Korner J; Lee WJ; Thomas AJ; Connett JE; Bantle JP; Leslie DB; Wang Q; Inabnet WB; Jeffery RW; Chong K; Chuang LM; Jensen MD; Vella A; Ahmed L; Belani K; Billington CJ
[Ad] Address:Department of Surgery, University of Minnesota, Minneapolis.
[Ti] Title:Lifestyle Intervention and Medical Management With vs Without Roux-en-Y Gastric Bypass and Control of Hemoglobin A1c, LDL Cholesterol, and Systolic Blood Pressure at 5 Years in the Diabetes Surgery Study.
[So] Source:JAMA;319(3):266-278, 2018 01 16.
[Is] ISSN:1538-3598
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Importance: The Roux-en-Y gastric bypass is effective in achieving established diabetes treatment targets, but durability is unknown. Objective: To compare durability of Roux-en-Y gastric bypass added to intensive lifestyle and medical management in achieving diabetes control targets. Design, Setting, and Participants: Observational follow-up of a randomized clinical trial at 4 sites in the United States and Taiwan, involving 120 participants who had a hemoglobin A1c (HbA1c) level of 8.0% or higher and a body mass index between 30.0 and 39.9 (enrolled between April 2008 and December 2011) were followed up for 5 years, ending in November 2016. Interventions: Lifestyle-intensive medical management intervention based on the Diabetes Prevention Program and LookAHEAD trials for 2 years, with and without (60 participants each) Roux-en-Y gastric bypass surgery followed by observation to year 5. Main Outcomes and Measures: The American Diabetes Association composite triple end point of hemoglobin A1c less than 7.0%, low-density lipoprotein cholesterol less than 100 mg/dL, and systolic blood pressure less than 130 mm Hg at 5 years. Results: Of 120 participants who were initially randomized (mean age, 49 years [SD, 8 years], 72 women [60%]), 98 (82%) completed 5 years of follow-up. Baseline characteristics were similar between groups: mean (SD) body mass index 34.4 (3.2) for the lifestyle-medical management group and 34.9 (3.0) for the gastric bypass group and had hemoglobin A1c levels of 9.6% (1.2) and 9.6% (1.0), respectively. At 5 years, 13 participants (23%) in the gastric bypass group and 2 (4%) in the lifestyle-intensive medical management group had achieved the composite triple end point (difference, 19%; 95% CI, 4%-34%; P = .01). In the fifth year, 31 patients (55%) in the gastric bypass group vs 8 (14%) in the lifestyle-medical management group achieved an HbA1c level of less than 7.0% (difference, 41%; 95% CI, 19%-63%; P = .002). Gastric bypass had more serious adverse events than did the lifestyle-medical management intervention, 66 events vs 38 events, most frequently gastrointestinal events and surgical complications such as strictures, small bowel obstructions, and leaks. Gastric bypass had more parathyroid hormone elevation but no difference in B12 deficiency. Conclusions and Relevance: In extended follow-up of obese adults with type 2 diabetes randomized to adding gastric bypass compared with lifestyle and intensive medical management alone, there remained a significantly better composite triple end point in the surgical group at 5 years. However, because the effect size diminished over 5 years, further follow-up is needed to understand the durability of the improvement. Trial Registration: clinicaltrials.gov Identifier: NCT00641251.
[Mh] MeSH terms primary: Gastric Bypass
Glycated Hemoglobin A/analysis
[Mh] MeSH terms secundary: Cholesterol, LDL/blood
Diabetes Mellitus, Type 2/blood
Female
Humans
Hypoglycemic Agents
Life Style
Middle Aged
Taiwan
Treatment Outcome
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; COMMENT
[Nm] Name of substance:0 (Cholesterol, LDL); 0 (Glycated Hemoglobin A); 0 (Hypoglycemic Agents)
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180118
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.20813

  10 / 41301 MEDLINE  
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[PMID]: 29273827
[Au] Autor:Uenishi K; Tokiwa M; Kato S; Shiraki M
[Ad] Address:Division of Nutritional Physiology, Kagawa Nutrition University, Saitama, Japan.
[Ti] Title:Stimulation of intestinal calcium absorption by orally administrated vitamin D3 compounds: a prospective open-label randomized trial in osteoporosis.
[So] Source:Osteoporos Int;29(3):723-732, 2018 Mar.
[Is] ISSN:1433-2965
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Intestinal fractional calcium absorption (FCA) was assessed before and after vitamin D3 treatment. Serum 1,25(OH) D concentration was significantly increased by plain vitamin D3 and reduced by eldecalcitol. The 1α hydroxyl calcidiol and eldecalcitol treatments increased FCA, which may be induced through direct stimulation of vitamin D receptors in the intestine. INTRODUCTION: To assess the effects of vitamin D3 compounds on intestinal FCA and calcium-regulating hormones in post-menopausal osteoporosis, a randomized open-label prospective study was conducted. METHODS: Forty eligible patients were allocated randomly into four groups: eldecalcitol (ELD; 0.75 µg/day), 1α hydroxyl calcidiol (ALF; 1 µg/day), plain vitamin D3 (800 IU/day), and control. Before and after the 4-week treatment, intestinal FCA was estimated by using a double isotope method, and serum concentrations of calcium-regulating hormones and a bone turnover marker were measured. RESULTS: The baseline FCA value of the participants was 21.5 ± 7.9% (mean ± SD) and was significantly correlated with serum 1,25(OH) D (calcitriol) concentration. After the treatment, the FCA significantly increased by 59.5% (95% CI, 41.6 to 77.4%) in the ELD group and by 45.9% (27.9 to 63.8%) in the ALF group, whereas no significant change in the plain vitamin D3 group was found. Unlike the baseline FCA, post-treatment FCA exhibited no significant correlation with serum calcitriol concentration. Parathyroid hormone levels were suppressed by ALF and plain vitamin D3 but were sustained in the ELD and control groups. Serum calcitriol tended to be suppressed by ELD, whereas plain vitamin D3 treatment increased both serum 25(OH)D and calcitriol concentrations. CONCLUSION: These findings suggest that oral administration of vitamin D3 analogues (ALF and ELD) stimulates FCA but plain vitamin D3 does not. Those effects of vitamin D3 compounds on FCA were independent of serum calcitriol concentration, suggesting that ALF and ELD may directly stimulate intestinal vitamin D receptors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1007/s00198-017-4351-2


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